ArticlePLoS pathogens2016
NK-CD11c+ Cell Crosstalk in Diabetes Enhances IL-6-Mediated Inflammation during Mycobacterium tuberculosis Infection.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Immune dysregulation in tuberculosis-diabetes comorbidity: mechanistic and translational insights.Frontiers in immunology · 2026Pooled it
- cAMP-response element binding protein (CREB)-mediated glycolysis enhancement promotes apoptosis of RAW264.7 macrophages infected with BCG under high glucose conditions.BMC microbiology · 2026Article
- Cell-mediated immune responses of beta-glucan on the pathogenesis of chronic tuberculosis infection.Frontiers in immunology · 2026Review
- Cytotoxic granules and effector molecules from immune cells in tuberculosis: Mechanisms of host defense and therapeutic potential.Virulence · 2025Review
- Impact of diabetes mellitus on tuberculosis prevention, diagnosis, and treatment from an immunologic perspective.Exploration (Beijing, China) · 2024Review
- Diabetes and tuberculosis: An emerging dual threat to healthcare.World journal of diabetes · 2024Article
- Metabolic changes enhance necroptosis of type 2 diabetes mellitus mice infected with Mycobacterium tuberculosis.PLoS pathogens · 2024Article
- Article
- Glycerol contributes to tuberculosis susceptibility in male mice with type 2 diabetes.Nature communications · 2023Article
- Host-directed therapy against mycobacterium tuberculosis infections with diabetes mellitus.Frontiers in immunology · 2023Review
- Immunologic, metabolic and genetic impact of diabetes on tuberculosis susceptibility.Frontiers in immunology · 2023Review
- Mouse Models forPathogens (Basel, Switzerland) · 2022Review
- Lnc-EST12, which is negatively regulated by mycobacterial EST12, suppresses antimycobacterial innate immunity through its interaction with FUBP3.Cellular & molecular immunology · 2022Article
- Early IL-17A production helps establish Mycobacterium intracellulare infection in mice.PLoS pathogens · 2022Article
- Cellular Immunity of Patients with Tuberculosis Combined with Diabetes.Journal of immunology research · 2022Review
- Pleiotropic Effect of IL-6 Produced by B-Lymphocytes During Early Phases of Adaptive Immune Responses Against TB Infection.Frontiers in immunology · 2022Article
- Impact of Diabetes Mellitus on the Immunity of Tuberculosis Patients: A Retrospective, Cross-Sectional Study.Risk management and healthcare policy · 2022Article
- Diabetes-Associated Susceptibility to Tuberculosis: Contribution of Hyperglycemia vs. Dyslipidemia.Microorganisms · 2021Review
- Effects of diabetes on the development of radiation pneumonitis.Respiratory research · 2021Review
- Clinical significance of cellular immunity function and inflammatory factors assays in alveolar lavage fluid for severe COVID-19 pneumonia.Journal of medical virology · 2021Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
In this study, we developed a mouse model of type 2 diabetes mellitus (T2DM) using streptozotocin and nicotinamide and identified factors that increase susceptibility of T2DM mice to infection by Mycobacterium tuberculosis (Mtb). All Mtb-infected T2DM mice and 40% of uninfected T2DM mice died within 10 months, whereas all control mice survived. In Mtb-infected mice, T2DM increased the bacterial burden and pro- and anti-inflammatory cytokine and chemokine production in the lungs relative to those in uninfected T2DM mice and infected control mice. Levels of IL-6 also increased. Anti-IL-6 monoclonal antibody treatment of Mtb-infected acute- and chronic-T2DM mice increased survival (to 100%) and reduced pro- and anti-inflammatory cytokine expression. CD11c+ cells were the major source of IL-6 in Mtb-infected T2DM mice. Pulmonary natural killer (NK) cells in Mtb-infected T2DM mice further increased IL-6 production by autologous CD11c+ cells through their activating receptors. Anti-NK1.1 antibody treatment of Mtb-infected acute-T2DM mice increased survival and reduced pro- and anti-inflammatory cytokine expression. Furthermore, IL-6 increased inflammatory cytokine production by T lymphocytes in pulmonary tuberculosis patients with T2DM. Overall, the results suggest that NK-CD11c+ cell interactions increase IL-6 production, which in turn drives the pathological immune response and mortality associated with Mtb infection in diabetic mice.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.